Abstract

Friday, August 19, 2016

Pipe dream?

Over the
last twenty years, half of all state legislatures have legalized marijuana for
medical purposes, such as controlling nausea among cancer patients. But
recently I came across a notion about marijuana that struck me as counterintuitive:
The drug’s active ingredient in marijuana, THC, may benefit people with
Alzheimer’s.

I was not much of a pot smoker as a teen, but I partook enough
times to learn that, unlike alcohol, the effect could be unpredictable. In
April 1979, a couple of friends and I drove the 90 miles to Seattle for the
day, and I was driving my dad’s gas-guzzling Chevrolet Malibu. Driving under
the influence, be it alcohol or marijuana, is never a good idea, but my timing
was especially bad. When I noticed that we were low on gas, I found my way to a
gas station, but it was nothing like I had ever seen. There were multiple lines
of at least a half-a-dozen cars ahead of us, and the lines showed little sign
of advancing. I was seventeen, the second energy crisis was at its peak, and I
interpreted the unmoving line of cars as an omen that civilization, like Jimmy
Carter’s presidency, was collapsing.

If I were to smoke pot these days, or, more likely, to
absorb the THC orally, I imagine it would be an act of piling mild confusion on
top of mild confusion. It is not unusual for me to forget why I entered a room
by the time I get there. But according to a press release earlier this summer
from the San Diego-area Salk Institute, THC can promote “the cellular removal
of amyloid beta”—also known as plaque, and assumed to be a key element in the
progression of Alzheimer’s. “Cellular” is the key word.

The Salk team studied nerve cells altered to produce high
levels of amyloid beta to mimic aspects of the disease. “The researchers found
that higher levels of amyloid beta were associated with cellular inflammation,”
the press release noted. While the tests involved neurons grown in
laboratories, “they may offer insight into the role of inflammation”—a
much-discussed topic among Alzheimer’s researchers. While other studies have
suggested that cannabinoids, THC in particular, offer protection from the
symptoms of the disease, “We believe our study is the first to demonstrate that
cannabinoids affect both inflammation and amyloid beta accumulation in nerve
cells,” according to David Salk.

A postdoctoral researcher working on the project, Antonio
Currais, was quoted as saying, “Inflammation is a major component of the damage
associated with Alzheimer’s, but it has
always been assumed that this response was coming from immune-like cells in the
brain, not the nerve cells themselves [my italics]. When we were able to
identify the molecular basis of amyloid beta, it became clear that THC-like
nerve cells may be involved in protecting the cells from dying.”

This was treated as good news, and I assume that in some
abstract way, it is. But as I was reading through my notes, I was hoping for
something less ambiguous than Currais’s cogent but not particularly promising
remark. The deflating word is “may.” So broad in implication. So unlikely to be
fulfilled through a cure anytime soon.